Preferential hydrolysis of peroxidized phospholipid by lysosomal phospholipase C

Gamache, Daniel A.; Fawzy, A. A.; Franson, Richard C.

doi:10.1016/0005-2760(88)90252-4

Cited by 46 publications

(10 citation statements)

References 30 publications

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“…35 The supplemented 12-or 15-HETE that elicited burst inhibition at micromolar concentration ( Figure 6) was, therefore, in the same concentration range as in trophozoiteor hemozoin-fed monocytes, even assuming incomplete hydrolysis of esterified OH-PUFAs by monocyte membrane phospholipase A 36 or by lysosomal phospholipases preferentially active on peroxidized phospholipids. 37 It is in fact possible that free OH-PUFAs as well as other toxic lipid derivatives were generated in the phagocyte, in analogy to the formation of large amounts of 4-hydroxynonenal previously observed in hemozoin-fed monocytes. 38 Other reported effects of 15-HETE may also point toward its role in malaria pathophysiology.…”

Section: Discussionmentioning

confidence: 91%

Malaria-parasitized erythrocytes and hemozoin nonenzymatically generate large amounts of hydroxy fatty acids that inhibit monocyte functions

Schwarzer

Kühn

Valente

et al. 2003

Blood

131

148

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Section: Discussionmentioning

confidence: 91%

Malaria-parasitized erythrocytes and hemozoin nonenzymatically generate large amounts of hydroxy fatty acids that inhibit monocyte functions

Schwarzer

Kühn

Valente

et al. 2003

Blood

131

148

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“…Enhanced prostaglandin synthesis due to increased phospholipase activity is likely since increased release of labeled arachidonic acid in histamine-stimulated irradiated cultures was present. UV-induced lipid peroxidation (24,25) may contribute to this increase in phospholipase activity since phospholipase stimulation and inhibition of fatty acid reacylation have been demonstrated in tissues suffering from peroxidation injury (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Pentland¹,

Mahoney²,

Jacobs³

et al. 1990

J. Clin. Invest.

116

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Acute ultraviolet light B (UVB) injury is associated with dermal mast cell histamine release. The possibility that histamine-stimulated prostaglandin (PG) synthesis could be a mechanism for irradiation erythema was therefore examined using human skin explants. Explants responded to UV irradiation (120 mJ/cm2) with a fivefold increase in synthesis of prostaglandins E2, F2. and 6-keto PGFIt. Incubating explants with the H1 antihistamines brompheniramine (50 MM) or pyrilamine (30 1AM) inhibited PG release from irradiated explants 63±4.9% (mean±SEM) 6 h after UV exposure. Antihistamines did not affect PG synthesis in control explants. Irradiation increased the histamine concentration in explant conditioned medium only 50% over basal values, suggesting that irradiation enhanced histamine responsiveness. Explants were therefore incubated with exogenous histamine. In irradiated explants, PG synthesis was stimulated threefold by 3 MM histamine. Unirradiated explants' PG synthesis was unaffected by histamine.Enhanced histamine sensitivity was also examined in epidermal cell cultures. In irradiated cultures, histamine sensitivity was again markedly potentiated: as little as 1 MM histamine stimulated significant PGE2 release and the response to 10-30 MAM histamine was increased six to eight times compared with that of unirradiated cultures. These studies demonstrate that endogenous histamine stimulates PG synthesis in human skin after UV injury by potentiation of histamine-induced prostaglandin release. Potentiated agonist responses induced by UV exposure may contribute to the effects of UVB irradiation injury and in particular to irradiation erythema. (J. Clin. Invest. 1990. 86:566-574.) Key words: ultraviolet light-skin -injury.

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“…In addition, lysosomal phospholipase C was identified from the soluble fractions of rat liver [17–19] and kidney [14] lysosomes, and canine cardiac sarcoplasmic reticulum [20]. The enzyme activity is characterized by has an acid pH optimum and the absence of any requirement for divalent metal ions.…”

Section: Phospholipid Metabolism In the Lysosomementioning

confidence: 99%

Drug induced phospholipidosis: An acquired lysosomal storage disorder

Shayman

Abe

2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

126

120

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There is a strong association between lysosome enzyme deficiencies and monogenic disorders resulting in lysosomal storage disease. Of the more than 75 characterized lysosomal proteins, two thirds are directly linked to inherited diseases of metabolism. Only one lysosomal storage disease, Niemann-Pick disease, is associated with impaired phospholipid metabolism. However, other phospholipases are found in the lysosome but remain poorly characterized. A recent exception is lysosomal phospholipase A2 (group XV phospholipase A2). Although no inherited disorder of lysosomal phospholipid metabolism has yet been associated with a loss of function of this lipase, this enzyme may be a target for an acquired form of lysosomal storage, drug induced phospholipidosis.

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Preferential hydrolysis of peroxidized phospholipid by lysosomal phospholipase C

Cited by 46 publications

References 30 publications

Malaria-parasitized erythrocytes and hemozoin nonenzymatically generate large amounts of hydroxy fatty acids that inhibit monocyte functions

Malaria-parasitized erythrocytes and hemozoin nonenzymatically generate large amounts of hydroxy fatty acids that inhibit monocyte functions

Enhanced prostaglandin synthesis after ultraviolet injury is mediated by endogenous histamine stimulation. A mechanism for irradiation erythema.

Drug induced phospholipidosis: An acquired lysosomal storage disorder

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